Malignant Catarrhal Fever (MCF) is an
infectious
disease of cattle,
bison, deer and other ruminants. (2) Relatively little is known about
MCF
in bison.

Cause

MCF is caused by viruses in the herpes
virus
family. In North American
bison the disease is associated with a virus that has never actually
been
isolated, but named Ovine herpes virus-2 (OHV-2) (2,5). It can be found
in most sheep and possibly goats, but does not cause clinical disease
in
these hosts (3,5). MCF caused by OHV-2 is therefore known as
sheep-associated
MCF (SA-MCF).

In Africa, a closely related virus called
Alcelaphine herpes virus-1
(AHV-1) is responsible for most cases. In 1960, the virus was isolated
and identified from the principal host and carrier of the virus, the
wildebeest
(10). MCF caused by AHV-1 is known as wildebeest-associated MCF
(WA-MCF).

A more recent discovery using DNA
technology for
typing disease causing
organisms is a herpes virus isolated from cases of MCF in white-tailed
deer (11). The virus has not yet been named because the reservoir or
carrier
species has not been recognized. Whether or not this virus also causes
disease in cattle, bison or other ruminants is not known but
researchers
have observed that there are no official reports of MCF in cattle or
bison
where either OHV-2 or AHV-1 has not been detected (12).

Geographic
distribution

MCF has a worldwide distribution (5).
However
most of the world's bison,
and therefore bison related cases of MCF, are found in North America.

The incidence of clinical MCF in wild
bison is
unknown. A serosurvey
for antibodies against OHV-2 in ranched bison from Montana and
Washington
showed positive titers in 2% of animals tested (3). Other researchers
have
placed this figure much higher at between 15 to 20% for the general
bison
population (9). Levels of serological evidence for MCF infection in
Canadian
bison have never been established. The high antibody prevalence rates
and
relatively low clinical disease rates suggest that many infections are
unapparent and non lethal. Seropositive animals and clinical MCF are
most
common in those regions farming bison under intensive management (12).

Transmission

There is strong evidence that sheep
carrying
OHV-2 virus are the primary
source of MCF. However, the mechanism of transmission of the virus from
sheep to bison is unknown (5). In some outbreaks there has been no
immediate
history of previous contact with sheep (9). This raises the possibility
of latent infection of bison with OHV-2 virus.

In sheep infection occurs early in life
with most
lambs being infected
via horizontal transmission from the mother or members of the flock by
the time they are six months of age. Since the virus is shed in nasal
secretions
of infected animals, bison are infected through contact with infected
sheep
and transfer of the virus from saliva or nasal secretions. Hay feeders,
common water sources, birds and care givers may facilitate virus
transmission
(16). Direct contact with sheep may not be necessary, as cattle and
bison
have apparently been infected by sheep held some distance away. This
suggests
windborne transfer of aerosolized virus, although this has never been
proven
(13).

Bison-to-bison transmission has not been
demonstrated. It is not known
if bison calves can become infected from seropositive mothers and herd
mates soon after birth as do sheep. OHV-2 is a cell-associated virus
and
bison and cattle have been infected experimentally by injection of
either
whole blood or white blood cells from a calf with MCF (1).

At one time bison and other species like
deer
were considered "dead
end" hosts, meaning that they were susceptible to infection but were
unable
to pass the infection to other individuals. The existence of MCF in
feedlot
cattle (14,15) and more recent outbreaks of MCF in feedlot bison (13)
with
no history of exposure to sheep have challenged this assumption.

Although OHV-2 has been associated or
linked with
MCF in bison there
are likely to be other factors involved in the development of MCF in a
bison. PCR testing (DNA test) for the presence of OHV-2 has shown that
not all persistently infected animals become diseased and die (12).
Other
viruses have been isolated from cases of MCF using PCR, although none
consistently.
Their role, if any, in the development of clinical disease is unknown
(17).
The incidence of MCF increases in winter and under intensive management
conditions. This suggests that stress or other factors that suppress
the
immune function may be necessary to develop clinical MCF (6).

Clinical signs

General clinical signs of MCF are
depression,
separation from the herd,
anorexia (not eating), incoordination, and persistent fever (40-410
C). There may be excessive salivation and nasal discharge due to
erosions
on the tongue and palate. Ocular discharge, conjunctivitis, and corneal
opacity are often observed. Affected animals may have diarrhea
(occasionally
with blood), or hematuria (bloody urine) (1,2,4). These signs can occur
in any combination, lasting from 1 to 4 days prior to death. Most
commonly,
bison infected with MCF are simply found dead. However, while the
clinical
course in bison is usually very rapid, there are reports of survival
for
months (2,9).

Post mortem
findings

Post mortem lesions vary considerably,
depending
on the severity and
course of the disease. Animals dying from per acute (rapid onset,
sudden
death) MCF have few lesions other than hemorrhagic enterocolitis (2).
In
cases of acute and subacute disease there are ulcerations throughout
the
alimentary tract and trachea, corneal opacity, conjunctivitis, enlarged
lymph nodes, and ulcerations or hemmorhage in the urinary bladder wall
(1,2,4,5).

Microscopic findings reflect the
lymphoproliferative nature of the disease.
Immune cells called lymphocytes infiltrate the tissue around blood
vessels
due to vasculitis (inflammation of blood vessels) and cause destructive
changes in organs such as the kidney and liver. These lymphoid cells
infiltrate
the liver and kidneys of most cases (2). Blocked blood vessels result
in
local cell necrosis (death) and inflammation leading to the ulcerations
in the upper respiratory, urinary and gastrointestinal tracts (2).

Diagnosis

A definitive diagnosis is made only by
microscopic examination of tissues
on post mortem. In live animals clinical signs and a detailed history
can
be used to form a presumptive diagnosis which needs to be supported by
laboratory tests. An OHV-2 specific test using DNA technology called
PCR
(Polymerase Chain Reaction) for the presence of virus can be done on an
unclotted blood sample. A recently developed but less reliable
serological
test for the presence of antibodies against OHV-2, called a
competitive-inhibition
ELISA test, can also be performed on blood serum. Interpretation of the
test results is not always straight forward. Positive ELISA or PCR
tests
in otherwise healthy animals do not seem to be indicators of impending
clinical disease and their significance is presently not well
understood
(3,17).

In dead animals the diagnosis depends upon
an
autopsy performed by a
veterinarian or a pathologist at a veterinary diagnostic laboratory. In
addition to the autopsy examination, tissue samples are taken for PCR
testing
and microscopic evaluation. The microscopic tissue changes in cases of
MCF are unmistakable. The typical lesions of MCF in addition to
positive
diagnostic tests form the diagnosis for MCF.

Differential
diagnosis

There are many diseases that cause sudden
death,
including rabies (8),
bloat, and anthrax. If the disease is more protracted, infectious
bovine
rhinotracheitis (IBR), bovine virus diarrhea (BVD), vesicular
stomatitis,
or foot and mouth disease might be confused with MCF unless appropriate
laboratory tests are performed.

Treatment

There is no effective treatment known for
MCF.
There is evidence that
supportive care with antibiotics and corticosteroids may prolong the
course
of disease (9) but the case fatality rate remains at or near 100%.

Prevention

There is no vaccine against MCF.
Prevention is
aimed at minimizing
risk factors associated with the occurrence of MCF. It is good practice
to avoid any contact with sheep and goats including wild varieties.
Minimize
the stress caused by inadequate diets and excessive handling or
inappropriate
handling techniques. There is evidence that bison can be infected with
OHV-2 for long periods of time, perhaps years, before developing
clinical
MCF (9). However, it may be wise to quarantine or segregate newly
acquired
animals from the main herd for at least one or two months.

Significance

MCF poses an economic threat to the bison
producer. Although outbreaks
of clinical MCF are uncommon and sporadic, the morbidity rate
(percentage
of animals that become sick) in infected herds is reported to be from 3
to 53 % (5) but can go as high as 100%. The mortality rate is almost
100%.